Smoking is a risk factor for a wide variety of conditions. In a recent study, investigators found that smoking is associated with more early evidence of interstitial lung disease than in healthy patients without rheumatoid arthritis (RA).1

“Smoking is likely just one of many environmental exposures that act in combination with host (genetic) factors to initiate RA [interstitial lung disease],” explained Cheilonda Johnson, MD, Instructor of Medicine, Department of Medicine, Division of Pulmonary and Critical Care Medicine, The Johns Hopkins University School of Medicine, Baltimore, MD, and colleagues. “Cigarette smoking, however, represents a major preventable risk factor for the development of RA [interstitial lung disease] and cessation efforts should be pursued aggressively.”

As part of this study, the investigators sought to determine whether smoking is associated with early evidence of interstitial lung disease. Study participants from the Evaluation of Subclinical Cardiovascular Disease and Predictors of Events in Rheumatoid Arthritis study and non-RA controls from the Multi-Ethnic Study of Atherosclerosis were enrolled in this analysis. Both studies were prospective in design, and evaluated subclinical and progressive subclinical cardiovascular disease. Similar criteria for inclusion and exclusion were included in both studies; patients ranged in age from 45 to 84 years. Cardiac multidetector row computed tomography scanning was performed in both groups at baseline. Other measures that were assessed include race/ethnicity, anthropometrics, and smoking history.

Overall, 172 patients with RA and 3969 non-RA controls had computed tomography densitometry data available. Looking at both study groups, the cohort of patients with RA tended to be younger and predominantly included white women; anthropometrically, both groups were similar; and patients with RA were significantly more likely to have smoked. In addition, mean RA duration was 8 years, with 38% of patients on prednisone therapy, 87% on nonbiologic disease-modifying antirheumatic drugs (DMARDs), and 46% on biologic DMARDs. Respiratory symptoms were present in 41% of patients, with 8% of the patients showing restrictive patterns on pulmonary function tests, and 17% demonstrating diffusing capacity impairment. The predicted mean forced vital and carbon monoxide diffusing capacity was 101%. Mean cumulative cigarette exposure was 25 in the RA group, compared with 15 pack-years in the control group.

Higher lung attenuation was associated with cigarette smoking. Specifically, the volume of high-attenuation areas was 0.03% higher for each 10 cigarette pack-year increment among patients with RA, compared with 0.008% in non-RA controls (P = .001). These trends became 0.02% and 0.005%, respectively, after adjusting for percent emphysema (P = .01). The investigators also found that areas of high attenuation were higher among patients with HLA-DRB1 shared epitope alleles who had greater smoking exposure.

Altogether, these data support Dr Johnson and colleagues’ hypothesis that cigarette smoking, together with other factors in patients with RA, increase the risk for interstitial lung disease. The study authors suggest that patients subtyped by anticyclic citrullinated peptide antibody positivity and negativity demonstrate distinct gene variation patterns and disease risk profiles by smoking status.